This study will investigate the role of traffic-related pollution in childhood asthma and lung function. The work[unreadable] will capitalize on findings from the southern California Children's Health Study (CHS), a population-based[unreadable] prospective cohort study. The CHS includes children from southern California communities that vary in[unreadable] regional air quality. We have found clinically significant lung function deficits, increased incidence of asthma,[unreadable] and increased respiratory symptoms among those living in communities with high regional pollution,[unreadable] compared to lower-pollution communities. We have found increased rates of prevalent and incident asthma[unreadable] and decreased lung function growth associated with indicators of traffic that vary within communities. These[unreadable] within-community associations with traffic indicators have been independent of the effects of regional[unreadable] pollution. We have also identified children susceptible to respiratory effects of oxidant pollutants, based on[unreadable] history of asthma, specific candidate genes, sex, in utero tobacco smoke exposure, and early life deficits in[unreadable] airway flow rates. We propose to build on these results by investigating the relationship between airways[unreadable] disease and specific traffic-related pollutants likely to be causing these effects. We hypothesize that[unreadable] respiratory effects will be linked to variation in toxicologically relevant components of particulate matter.[unreadable] including transition metals and total and water soluble organic carbon, which will be measured in different[unreadable] size fractions (PM[0.25], PM[0.25-2.5] and PM[2.5-10]). We will examine (1) associations of these specific traffic-related[unreadable] pollutants and gaseous co-pollutants with well-characterized incident asthma and with lung function[unreadable] level and growth; and (2) modification of the effect of traffic-related pollutant effects on lung function growth[unreadable] by asthma and exhaled nitric oxide (eNO, a marker of airway inflammation). In addition, we will jointly model[unreadable] respiratory outcomes, including asthma, lung function, and other available respiratory health indicators[unreadable] including eNO, that may reflect vulnerability to effects of particulate air pollution. Longitudinal lung function[unreadable] will be measured in 1,900 children between approximately 11 and 15 years of age and new-onset asthma[unreadable] cases will be identified. Particulate and gaseous pollutants will be monitored at multiple locations within each[unreadable] of eight study communities that have large within-community gradients in traffic and between-community[unreadable] variation in regional air quality. Long-term average exposures will be estimated for each child, using state-of-[unreadable] the-art GIS methods and spatial modeling. This study will further our understanding of the childhood[unreadable] origins of obstructive lung disease and has important implications for development of interventions and[unreadable] regulatory policy, since traffic is a common exposure and asthma and chronic obstructive pulmonary disease[unreadable] are major public health problems.